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Clinical Pathology 2017 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Leakage enzymes

A

CK, AST, ALT, SDH, GLDH

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2
Q

Induction enzymes

A

ALP, GGT

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3
Q

CK sources and half-life

A

Sources: skeletal, cardiac and smooth muscle; brain (highly specific/sensitive for myopathies)
Half-life: very short (hrs)

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4
Q

AST sources and half-life

A

Sources: skeletal muscle and hepatocytes mainly; also RBCs, other cells (sensitive, low specificity)
Half-life: hours/days

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5
Q

ALT sources and half-life

A

Sources: hepatocytes mainly, also skeletal muscle in dogs/cats (very specific/sensitive for liver, rarely increases with myopathy)
Half-life: hours/days

small animals only

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6
Q

SDH sources and half-life

A

Sources: hepatocytes
Half-life: hours

horses, ruminants, swine

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7
Q

GLDH sources and half-life

A

Sources: hepatocytes
Half-life: hours

large animals and exotics

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8
Q

Enzymes increased with myopathy (muscle disease)

A

CK, AST, ALT

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9
Q

Enzymes increased with hepatocellular injury

A

AST, ALT, SDH

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10
Q

Liver disease: all hepatic enzymes

A

Leakage: ALT, AST, SDH

Induced/cholestasis: ALP, GGT

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11
Q

Markers for cholestasis

A

Bilirubin, bile acids, cholesterol, ALP, GGT

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12
Q

Hepatic function tests and what happens with decreased liver function

A

Synthetic function tests: albumin
- albumin, BUN, cholesterol, glucose
- decreased liver function = decreased synthetic function tests (can’t make)
Excretory function tests: bilirubin
- bilirubin, bile acids, ammonia
- decreased liver function = increased excretory function tests (can’t excrete)

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13
Q

What causes elevated inducible enzymes (cholestatic enzymes)?

A

Increased synthesis from hyperplastic cells

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14
Q

ALP sources and half-life

A

Sources: hepatocytes, biliary epithelium, osteoblasts, colostrum (low specificity)
Half-life: dog 3 days, cat 6 hours

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15
Q

GGT sources and half-life

A

Sources: biliary epithelium mainly; also hepatocytes and colostrum (more specific for cholestasis than ALP)
Half-life: 3 days

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16
Q

Which enzymes are more sensitive to cholestasis (by species)?

A

Dog: ALP
Cat, horse, cattle: GGT
(in cats and horses, bilirubin increases before ALP)

ALP = more specific for all

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17
Q

Other considerations for elevated induced enzymes: ALP, GGT

A

Ingestion of colostrum in dogs, cats, ruminants
Steroids or PB use in dogs
ALP only: younger than 1 yr, or osteosarcoma

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18
Q

Pre-hepatic bilirubinemia

A

Mostly unconjugated increased

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19
Q

Causes of pre-hepatic bilirubinemia

A

Hemolytic disease

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20
Q

Hepatic bilirubinemia

A

Mixed conjugated and unconjugated

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21
Q

Causes of hepatic bilirubinemia

A

Defective uptake of unconjugated bilirubin: hepatic dysfunction, anorexia in horses
Defective conjugation/excretion of bilirubin: hepatic dysfunction, functional cholestasis (sepsis), intra and extra-hepatic cholestasis

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22
Q

Post-hepatic bilirubinemia

A

Mostly conjugated bilirubin increased

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23
Q

Unconjugated vs conjugated bilirubin

A 
Unconjugated = binds to albumin, accumulates in blood
Conjugated = water soluble, accumulates in urine
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24
Q

What increase occurs first, hyperbilirubinemia or bile acids?

A

Hyperbilirubinemia

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25
Q

Different tests for bilirubin

A 
Total bilirubin (routine chem)
Bilirubin splits (direct = conjugated, indirect = unconjugated - good for anorexic horses)
Urinary bilirubin (urine dipstick, never normal in cat)
Urinary urobilinogen (not clinically important)
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26
Q

Bile acid metabolism

A 
Synthesized by hepatocytes from cholesterol
Conjugates and excreted into bile
Stored in gall bladder
CCK releases into duodenum
Reabsorbed by ileum (portal vein)
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27
Q

Process of bile acid metabolism requires 3 working parts:

A
  1. Healthy hepatocytes
  2. Intestinal absorption
  3. Portal circulation
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28
Q

Causes of increased bile acids

A

Decreased hepatic clearance: portosystemic shunt or microvascualr dysplasia
Hepatocellular dysfunction
Decreased hepatic biliary excretion: intra/extra-hepatic cholestasis, functional cholestasis (sepsis)
Maltese dogs: normal

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29
Q

Indication for bile acid tests

A

When hepatic enzymes/function tests are minimally altered, but liver disease suspected
NOT indicated with hyperbilirubinemia

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30
Q

Procedure for testing bile acids

A

1 fasted sample, 1 post-prandial sample (after gallbladder contraction, 1 sample in horses)

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31
Q

Ammonia source and clearance

A

Protein degradation by enteric bacteria, absorbed by intestines, cleared from portal circulation by hepatocytes via urea cycle

32
Q

Significance of hyperammonemia

A

Accumulates during liver dysfunction - hepatocytes not converting ammonia to urea (increased ammonia, decreased BUN)
Role in hepatic encephalopathy

33
Q

Causes of hyperammonemia

A

Decreased blood clearance: hepatocellular dysfunction (decreased uptake), PSS, urea cycle disorders
Increased production/intake: physiologic, urea toxicosis (cattle), intestinal disease (horses)

34
Q

Analytes synthesized by hepatocytes = DECREASED WITH HEPATIC DYSFUNCTION

A

Albumin (late liver disease)
Urea
Cholesterol (may be increased with concurrent cholestasis)
Glucose (late liver disease, may be increased with decreased hepatic intake)
Clotting factors

35
Q

BUN:Creat change with disease

A

High with pre-renal azotemia or GI hemorrhage

36
Q

Total protein change with disease

A

Low with PLE - both albumin and globulins are low

37
Q

Cholesterol changes with disease

A

Low with PLE

38
Q

Calcium change with disease

A

Low with intestinal malabsorption or secondary to hypoalbuminemia

39
Q

Magnesium change with disease

A

Low with decreased intake (anorexia) or decreased GI absorption

40
Q

Phosphorous change with disease

A

Low with decreased intake (anorexia) or decreased GI absorption

41
Q

Sodium changes with disease

A

High if pure water loss by GI tract

Low if isotonic fluid or Na rich fluid loss by GI tract

42
Q

Potassium changes with disease

A

Low if lost in GI or anorexia

43
Q

Chloride changes with disease

A

High if pure water loss by GI
Low if isotonic fluid or CL rich fluid loss by GI
Disproportionally elevated relative to Na if HCO3 being lost by GI

44
Q

TCO2 changes with disease

A

High with upper GI disease and selective loss of HCl

Low if losing bicarbonate in diarrhea

45
Q

Protein changes with hemorrhage, BLE, exudative lesion, SEVERE PLN or hepatopathy

A

Panhypoproteinemia

46
Q

Protein changes with PLN or hepatopathies

A

Hypoalbuminemia

47
Q

Protein changes with inflammation, hepatopathies

A

Hypoalbuminemia

Hyperglobulinemia

48
Q

Protein changes with dehydration

A

Panhyperproteinemia

49
Q

Pancreatitis: CBC changes

A

Neutrophilia with L shift +/- toxicity
Lymphopenia
Eosinopenia
Thrombocytopenia

50
Q

Pancreatitis: chem changes

A

Hypercholesterolemia
Increased ALT (liver leakage), ALP (cholestatic)
Hyper bilirubinemia d/t cholestasis
Hypocalcemia (more so in cats)
Hyperglycemia (hyperglucagonemia - alpha cells of pancreas, diabetes, stress)

51
Q

Clinical signs of pancreatitis in dogs vs cats

A

Dogs: pain, V/D, fever
Cats: dehydration, weight loss, hypothermic, icterus (less likely to see V and fever)

52
Q

Exocrine pancreatic insufficiency (EPI)

A

Insufficient synthesis/secretion of digestive enzymes by pancreatic acinar tissue = maldigestion

53
Q

Clinical signs of EPI

A

Chronic, severe weight loss despite and GOOD APPETITE

Cow patty diarrhea

54
Q

Additional complications of EPI (3)

A 
Concurrent with diabetes mellitus
Secondary SIBO (lack of anti-bacterial factor or bicarbonate from pancreas)
Secondary cobalamin/B12 deficiency (lack of IF from pancreas)
55
Q

EPI: CBC changes

A

Maybe normal

+/- normocytic, normochromic anemia

56
Q

EPI: chem changes

A

Often normal
+/- low cholesterol
+/- hyperglycemia
+/- mild to moderate elevated ALT, AST, ALP

57
Q

Pancreatic enzymes

A

Amylase, lipase, trypsin

58
Q

Which pancreatic enzymes are decreased with EPI?

A

Lipase and trypsin

59
Q

Amylase sources

A

Pancreatic acinar cells*, SI, salivary glands in pigs

60
Q

Lipase sources

A

Pancreatic acinar cells*, gastric mucosal cells, SI, liver, adipocytes, myocytes

61
Q

Trypsin sources

A

Pancreatic acinar cells, as trypsinogen

62
Q

Causes of elevated amylase

A

Pancreatic disease, GI disease, renal failure, other causes of decreased GFR ( pre and post-renal)

63
Q

Causes of elevated lipase

A

> 3 fold = likely pancreatitis

64
Q

Causes of elevated trypsin

A

Pancreatitis, pancreatic hypertrophy, renal disease, SI disease

65
Q

What are each of the pancreatic enzymes tests used for?

A

Amylase: increases seen with pancreatitis, pancreatic neoplasia, enteritis
Lipase: used to dx pancreatitis
Trypsin: used to dx EPI

66
Q

Maldigestion vs. malabsorption

A 
Maldigestion = think pancreas
Malabsorption = think GI
67
Q

Malabsorption

A

Thickened GI = abnormal cell infiltration d/t inflammation/cancer
Parasitism/infection
GI lymphatic disease = lymphangestasia

CS: V/D, colic, abomasal disease

68
Q

Effect of EPI on folate, cobalamin, TLI

A

Folate: normal/increased
Cobalamin: decreased
TLI: decreased

69
Q

Effect of bacterial overgrowth on folate, cobalamin, TLI

A

Folate: increased
Cobalamin: decreased
TLI: normal

70
Q

Effect of proximal SI disease on folate, cobalamin, TLI

A

Folate: decreased
Cobalamin: normal
TLI: normal

71
Q

Effect of distal SI disease on folate, cobalamin, TLI

A

Folate: normal
Cobalamin: decreased
TLI: normal

72
Q

Effect of diffuse SI disease on folate, cobalamin, TLI

A

Folate: decreased
Cobalamin: decreased
TLI: normal

73
Q

Folate vs cobalamin

A

Folate = B9
- produced by bacteria, increased with ARE, absorbed in proximal SI
Cobalamin = B12
- absorption decreased by bacteria, decreased with ARE, absorbed in duodenum and mostly ileum with IF from pancreas

74
Q

Causes of hypocholesterolemia

A

Decreased hepatic synthesis = hepatic disease, PSS
Decreased intestinal absorption = PLE
Maldigestion = EPI

75
Q

Clinical signs of hypoglycemia

A

Lethargy, incoordination, exercise intolerance, seizures, coma

76
Q

Causes of hypoglycemia

A

Increased insulin secretion (insulinoma, xylitol toxicity)
Decreased insulin antagonists (cortisol)
Decreased gluconeogenesis (liver insufficiency, dec cortisol, starvation)
Increase glucose utilization (lactational, exertional)
Sepsis/neoplasm
Pharmacological (insulin, sulfonylurea)

77
Q

Causes of hyperglycemia

A

Catecholamine induced (fractious animal, pheochromocytoma)
Endocrine (DM, Cushing’s, acromegaly, hyperpituitarism)
Drugs (dextrose, xylazine, ketamine)
Hyperglucagonemia (glucagonoma)
Pancreatitis
Other

Clinical Pathology 2017 (4 decks)

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